Congratulations to John Conduah of the Onukwufor lab for receiving both a Dekiewiet Summer Research Fellowship and Schwartz Discover Grant
Thursday, April 10, 2025
These awards will fund John’s summer research project and help elucidate how interactions between Cd, Pb and Fe contribute to mechanisms of acute metal toxicity and liver mitochondrial dysfunction.
Congratulations to Michael Malloy as the recipient of a two-year Predoctoral Fellowship from the American Heart Association
Wednesday, January 1, 2025
Michael Malloy, 3rd year graduate student in the laboratory of Dr. Craig Morrell was awarded a two-year American Heart Association Predoctoral Fellowship entitled, “Myb regulation of megakaryocyte immune differentiation”.
Project Summary
Lung megakaryocyte (Mk) derived platelets have been described throughout the past century. Our laboratory previously reported that lung Mks are transcriptionally distinct from bone marrow (BM) Mks and have an immune differentiated phenotype and functions. A recent manuscript from our lab discovered that lung Mks originate from the BM and a developmentally distinct population migrate to the lung. Part of our lab’s current efforts seek to identify the developmental cues and molecular mediators that facilitate the differentiation of Mks fated to stay in the BM or become immune differentiated and travel to the lung. As part of these efforts, I identified a novel mediator of Mk immune differentiation, the protooncogene Myb, that regulates the immune phenotype of Mks in both the BM and lung. My work has now found that the majority of BM, but not lung Mks, express the transcription factor, Myb, that may limit Mk immune differentiation, impacting the functions of both lung vs BM derived platelets.
Congratulations to Nada Ahmed Selim on receiving the Predoctoral Fellowship from the American Heart Association!
Wednesday, January 1, 2025
Nada Ahmed Selim, 4th year graduate student in the laboratory of Dr. Andrew Wojtovich was awarded a two-year American Heart Association Predoctoral Fellowship entitled, “Optogenetic regulation of mitochondria to improve ischemiareperfusion injury outcomes”.
Project Summary
Mitochondria coordinate metabolism, ATP synthesis, and cell death, and their function is essential for neuronal survival and post-stroke recovery. Mitochondria are powered by the electron transport chain (ETC), which creates an electrochemical protonmotive force (PMF) across the inner mitochondrial membrane that drives oxidative phosphorylation to generate ATP. The PMF is essential for neuronal function, and its disruption adversely affects neurons through poorly understood mechanisms. PMF responds rapidly to energy demands and stress, signaling metabolic needs. During ischemia-reperfusion (IR) injury, the PMF decreases and then is restored upon reperfusion. The rapid change in PMF during IR is associated with numerous pathological events at the mitochondrial level, such as excessive production of reactive oxygen species (ROS), calcium overload, and subsequent initiation of cell death cascades.